Monita Karmakar
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Monita Karmakar has a total of 14 co-authors. Here are the top co-authors by number of shared publications:
- Arulselvi Subramanian
Department of Laboratory Medicine, Jai Prakash Narayan Apex Trauma Center, All India Institute of Medical Sciences, New Delhi, India
1 shared publication - Arun Anantharam
Department of Neurosciences, University of Toledo, Toledo, OH 43614
1 shared publication - Bethany Beilue Moore
Department of Microbiology and Immunology, University of Michigan, Ann Arbor, MI, USA
1 shared publication - Bivin Thomas
Department of Surgery, University of Michigan, Ann Arbor, Michigan, USA
1 shared publication - Boya Zhang
Department of Surgery, University of Michigan, Ann Arbor, Michigan, USA
1 shared publication - David Machado-Aranda
Department of Surgery, University of Michigan, Ann Arbor, Michigan, USA
1 shared publication
Latest Publications
- 5 December 2019
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 4 (23)
TLR3 absence confers increased survival with improved macrophage activity against pneumonia
Toll-like receptor 3 (TLR3) is a pathogen recognition molecule associated with viral infection with double-stranded RNA (dsRNA) as its ligand. We evaluated the role of TLR3 in bacterial pneumonia using Klebsiella pneumoniae ( KP ). WT and TLR3 –/– mice were subjected to a lethal model of KP . Alveolar macrophage polarization, bactericidal activity, and phagocytic capacity were compared. RNA-sequencing was performed on alveolar macrophages from the WT and TLR3 –/– mice. Adoptive transfers of alveolar macrophages from TLR3 –/– mice to WT mice with KP were evaluated for survival. Expression of TLR3 in postmortem human lung samples from patients who died from gram-negative pneumonia and pathological grading of pneumonitis was determined. Mortality was significantly lower in TLR3 –/– , and survival improved in WT mice following antibody neutralization of TLR3 and with TLR3/dsRNA complex inhibitor. Alveolar macrophages from TLR3 –/– mice demonstrated increased bactericidal and phagocytic capacity. RNA-sequencing showed an increased production of chemokines in TLR3 –/– mice. Adoptive transfer of alveolar macrophages from the TLR3 –/– mice restored the survival in WT mice. Human lung samples demonstrated a good correlation between the grade of pneumonitis and TLR3 expression. These data represent a paradigm shift in understanding the mechanistic role of TLR3 in bacterial pneumonia.
- 5 December 2019
- Published by American Society for Clinical Investigation in JCI Insight
- Vol. 4 (23)
TLR3 absence confers increased survival with improved macrophage activity against pneumonia
Toll-like receptor 3 (TLR3) is a pathogen recognition molecule associated with viral infection with double-stranded RNA (dsRNA) as its ligand. We evaluated the role of TLR3 in bacterial pneumonia using Klebsiella pneumoniae ( KP ). WT and TLR3 –/– mice were subjected to a lethal model of KP . Alveolar macrophage polarization, bactericidal activity, and phagocytic capacity were compared. RNA-sequencing was performed on alveolar macrophages from the WT and TLR3 –/– mice. Adoptive transfers of alveolar macrophages from TLR3 –/– mice to WT mice with KP were evaluated for survival. Expression of TLR3 in postmortem human lung samples from patients who died from gram-negative pneumonia and pathological grading of pneumonitis was determined. Mortality was significantly lower in TLR3 –/– , and survival improved in WT mice following antibody neutralization of TLR3 and with TLR3/dsRNA complex inhibitor. Alveolar macrophages from TLR3 –/– mice demonstrated increased bactericidal and phagocytic capacity. RNA-sequencing showed an increased production of chemokines in TLR3 –/– mice. Adoptive transfer of alveolar macrophages from the TLR3 –/– mice restored the survival in WT mice. Human lung samples demonstrated a good correlation between the grade of pneumonitis and TLR3 expression. These data represent a paradigm shift in understanding the mechanistic role of TLR3 in bacterial pneumonia.